Estradiol promotes luteal regression through a direct effect on the ovary and an indirect effect from the celiac ganglion via the superior ovarian nerve.

MARILINA CASAIS; SANDRA S. VALLCANERAS; FIORELLA CAMPO VERDE ARBOCCO; SILVIA M. DELGADO; MARIA B. HAPON; ZULEMA SOSA, PHD; CARLOS M. TELLERIA; ANA M. RASTRILLA

REPRODUCTIVE SCIENCES

SAGE PUBLICATIONS INC

Lugar: Thousand Oaks, California.; Año: 2012 vol. 19 p. 416 - 422

1933-7191

There is evidence suggesting that estradiol (E2) regulates the physiology of the ovary and the sympathetic neurons associated with the reproductive function. The objective of this study was to investigate the effect of E2 on the function of late pregnant rat ovaries, acting either directly on the ovarian tissue or indirectly via the superior ovarian nerve (SON) from the celiac ganglion (CG). We used in vitro ovary (OV) or ex vivo CG-SON-OV incubation systems from day 21 pregnant rats. Various concentrations of E2 were added to the incubation media of either the OV alone or the ganglion compartment of the CG-SON-OV system. In both experimental schemes, we measured the concentration of progesterone in the OV incubation media by radioimmunoassay at different times. Luteal messenger RNA (mRNA) expression of 3β-hydroxysteroid dehydrogenase (3β-HSD) and 20α-hydroxysteroid dehydrogenase (20α-HSD) enzymes, respectively, involved in progesterone synthesis and catabolism, and of antiapoptotic B-cell lymphoma 2 (Bcl-2) and proapoptotic Bcl-2-associated X protein (Bax), were measured by reverse transcriptase?polymerase chain reaction (RT-PCR) at the end of the incubation period. Estradiol added directly to the OV incubation or to the CG of the CG-SON-OV system caused a decline in the concentration of progesterone accumulated in the incubation media. In addition, E2, when added to the OV incubation, decreased the expression of 3β-HSD and the ratio of Bcl-2/Bax. We conclude that through a direct effect on the OV, E2 favors luteal regression at the end of pregnancy in rats, in association with neural modulation from the CG via the SON.